Renal compensatory growth, after the loss of functioning parenchyme due to nephrectomy or hydronephrosis, is an important clinical phenomenon which often eventually results in glomerulosclerosis and renal failure. Thus numerous efforts have been
made to
elucidate the mechanism of compensatory growth and to discover the methods which can impede the compensatory process. Compensatory renal growth in mature animals is mainly by cellular hypertrophy, the increase in cellular component without
increase
in
number of cell. But small portion of growth is composed of hyperplasia, the increase in total number of cells.
To evaluate hyperplasia and hypertrophy, flow cytometry is employed. The DNA ploidy pattern of each kidney cell is analyzed, and the proportion of synthetic and replicating cells is calculated. For evaluation of hypertrophy, the presumed
causative
metabolite, nitric oxide, is indirectly titrated by measuring the activity of its key enzyme, intric oxide synthase. The results of the experiment are as follows.
1. The increase in fraction of synthetic and replicating cells in flow cytometry is a definite evidence of cellular hyperplasia, thus hyperplasia is involved in neonatal compensatory renal growth.
2. Cellular hyperplasia is profound after 48 to 72 hours of injury.
3. A statistically significant difference was noted at 12 hours after nephrectomy between control and experimental groups in G2 + m phase (mitotic phase).
4. Nitric oxide is an important messenger of early (within 48 hours) renal compensatory growth in neonatal rats.
5. In view of the adult model experiment of nitric oxide synthase, where nitric oxide is confirmed to be involved in renal compensatory hypertrophy, nitric oxde is also related to the renal hypertrophy in neonatal periods.
In conclusion, the compensatory renal growth in neonatal period is due to both hyperplasia and hypertrophy. Nitric oxide is a key signalling messenger of early compensatory renal growth, it can be stated that if the process of hypertrophy could
be
selectively blocked, prevention of renal failure as a consequence of glomerulosclerosis can be a reality.
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